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Introduction

ECG Challenge: A 26-year-old man without any known heart disease reports intermittent palpitations that last for several minutes and he thinks terminate with coughing. He has been seen several times in an emergency department, but no etiology for the palpitations has been established. His baseline ECG is seen (ECG A). He has an episode of palpitations that lasts several hours that prompts another visit to the emergency department. An ECG during the palpitations is recorded (ECG B).

ECG A shows a regular rhythm at a rate of 60 bpm. There is a P wave before each QRS complex (+) with a stable but short PR interval (0.12 s). The P waves are positive in leads I, II, aVF, and V4 through V6. Therefore, this is normal sinus rhythm. The QRS complexes have an increased duration (0.12 s) and this is the result of a slurring of the QRS upstroke (↑) which widens the base of the QRS complex while the peak is narrow. This slurring is known as a delta wave and is caused by preexcitation resulting from early and direct myocardial activation via an accessory pathway. Along with the short PR interval, the QRS complex is diagnostic of a Wolff-Parkinson-White (WPW) pattern. In addition, there is positive concordance, ie, a tall R wave from V1 through V6 (←). Positive concordance is not the result of conduction through the His-Purkinje system but is attributable to direct myocardial activation. It may be seen with a ventricular complex, ventricular paced complex, or a WPW complex. The axis is normal between 0° and 90° (positive QRS complex in leads I and aVF). The QT/QTc intervals are normal (400 ms/400 ms and 380 ms/380 ms when corrected for the prolonged QRS complex duration). There is 1 premature complex (^) and it is preceded by a P wave (*), which has a slightly different morphology than the sinus P wave. This is a premature atrial complex. The QRS complex has the same morphology as the sinus complexes, but is it wider (0.14 s) or more preexcited. The premature atrial impulse is associated with slower conduction via the atrioventricular (AV) node because of decremental conduction. Because the WPW complex is the result of fusion with early myocardial activation via an impulse conducted through the accessory pathway fusing with activation via the normal AV node His-Purkinje system, the conduction through the AV node will determine the degree of preexcitation. When AV nodal conduction is slower, as with the premature atrial complex, more of the ventricular myocardium is activated via the accessory pathway, resulting in more preexcitation and a wider QRS complex. Another explanation to account for the increase in preexcitation is that the premature atrial complex originates closer to the accessory pathway.

ECG B shows a regular rhythm at a rate of 148 bpm. The QRS complex is wide (0.12 s) with a typical right bundle-branch block pattern, ie, RSR′ complex in lead V1 (→) and a broad terminal S wave in leads I and V5 to V6 (↑). The axis is normal between 0° and 90° (positive QRS complex in leads I and aVF).The QT/QTc intervals are normal (280 ms/440 ms and 260 ms/410 ms when corrected for the prolonged QRS complex duration). Although there are no P waves seen before any of the QRS complexes, there are regular notches seen after each QRS complex, within the ST segment (*), particularly in leads II, aVR, aVL, and V5 to V6. These notches have a stable relationship to the QRS complex. These are P waves that are negative in leads II and V5 to V6 and are positive in lead aVR. It can be seen that this is a short RP tachycardia because the RP interval is shorter than the PR interval. There are several etiologies for a short RP tachycardia:

Sinus tachycardia with a long PR interval; this is not the etiology, because the P waves are negative in leads II and V5 to V6 and positive in lead aVR.

Atrial flutter with 2:1 AV block, which is not likely because a second flutter wave is not seen

Because the patient has a known WPW pattern on the baseline ECG, it is most likely that the arrhythmia is an AVRT. Although the QRS complex is wide, this is not an antidromic AVRT. With antidromic AVRT, ventricular activation is via the accessory pathway, whereas retrograde conduction to the atria is via the normal His-Purkinje-AV nodal pathway. Therefore the QRS complex will be maximally preexcited and will resemble the morphology of the preexcited sinus complex. In this case, the QRS complex of the tachycardia has a typical right bundle-branch block morphology, which is different from the WPW or preexcited sinus QRS complex seen in ECG A. Importantly, it is very different from the premature atrial complex in ECG A that is maximally preexcited. Therefore, this is an orthodromic AVRT with a right bundle-branch block aberration (either rate related or preexisting). With an orthodromic AVRT, ventricular activation is via the normal AV node His-Purkinje system, whereas retrograde conduction is via the accessory pathway.

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